Ch. 16 Innate Immunity: Nonspecific Defenses of the Host

Question 1

Mechanisms of the innate immunity

Answer 1

Its a “standing army” and its functions are more general than specific.

Question 2

1st line defense

Answer 2

Skin, m membranes, etx. sometimes breached

Question 3

2nd line of defense

Answer 3

Fever, inflammation

Question 4

3rd line of defense

Answer 4

humoral and cell immunity

Question 5

1st line defenses

Answer 5

Physical, chemical, normal microbiota. mucous (entraps microbes to flush them out). tears (prevent pathogens from attaching to eyes).

Question 6

Normal microbiota

Answer 6

• Perform microbial antagonism.
• Compete for nutrients and crowd out pathogens.
• Some produce substances that are harmful to pathogens.
• they alter environment. pH for example.
• necessary for the development of the immune system. Hygiene hypothesis.

Question 7

Phagocytosis

Answer 7

• Neutrophils and macrophages.

Question 8

Steps of phagocytosis (step 1)

Answer 8

1. Phagocyte attaches to pathogen. Bacteria has to have receptors on it (ligands) for the phagocyte to recognize it.

side note: PRRs pattern recognition receptors = recognize attributes of bacteria that human cells do not have. Like peptidoglycan and flagellum.

side note 2.0: Pathogen associated molecular pattern (PAMPs) are these patterns that phagocytes recognize.

Capsules can inhibit recognition of these PAMPs.

Question 9

Steps of phagocytosis (step 2)

Answer 9

2. Engulfment. Bacteria in a vesicle inside cytoplasm. Cytosome. Lysozomes fuse with phagosome to become a phagolysozome. Then pathogen is “digested”.

Question 10

Steps of phagocytosis (step 3)

Answer 10

3. Bits and pieces of pathogen get dumped outside of cell.

Question 11

Inflammation

Answer 11

• Response to tissue damage.

- Brings effectors to site of infection that help with tissue repair

Question 12

A series of responses in inflammation

Answer 12

• Clears infection and repairs. increases blood flow and anti-microbes
• Typically localized inflammation

Question 13

Systemic infection

Answer 13

• Fever
• Bacterial endotoxins (pyrogens) (lipid A)
• IL-1 and TNF - a

Question 14

Complement initiation – results of complement activation

Answer 14

Its a series of 9 proteins that are always in an inactive form (1 - 9). They are activated when an acute infection occurs. So its innate.

Question 15

3 pathways – classical pathway

Answer 15

Discovered first. Only know step one –>

antibodies bind to antigen and it starts. Plays later in immune response. the three pathways work together.

Question 16

Alternative pathway

Answer 16

Discovered 2nd. Plays in before use of antibodies. Factor B,D, and E bind to antigens on microbe. Complement then binds to those proteins.

Question 17

Lectin pathway

Answer 17

Binds to a carbohydrate. MBL binds to carbs on bacteria cell surface. Allows binding of complement proteins.

Question 18

Outcomes of complement pathways

Answer 18

1. Cytolysis. bursting of gram-neg bacteria.
2. Opsonization: an immune process which uses opsonins to tag foreign pathogens for elimination by phagocytes.
3. Inflammation. Complement proteins promote it. Blood vessels become more permeable. Binding on mast cells to release granules like histamine to assist.

Question 19

Interferons

Answer 19

Interfere with viruses. there is an alpha and beta verions. a-INF and b-INF. Any cell can make these a & b INFs. Once a cell is infected these don’t help, and they don’t cure the infected cell.

Question 20

INFs.

Answer 20

Slow the spread of viral infections by protecting neighboring cells.

Question 21

How does a cell know its infected, and to produce INFs?

Answer 21

Long double strand RNA in host cytoplasm produced during virus life cycle alerts it

Question 22

The process of INFs alerting neighboring cells (fig 16.14)

Answer 22

1. Viral DNA from an infecting virus enters the cell
2. The virus induces the host cell to produce interferon mRNA (INF-mRNA), which is translated into alpha and beta interferons.
3. Interferons make contact with uninfected neighboring host cells, where they bind either to the plasma membrane or to nuclear receptors. Interferons induce the cells to synthesize antiviral proteins (AVPs).
4. AVPs degrade viral mRNA and inhibit protein synthesis – and thus interfere with viral replication.

Question 23

Iron binding proteins

Answer 23

• Competition with pathogens

- Antimicrobial peptides (AMPs) triggered by carbs/proteins on microbes.

Question 24

Modes of action

Answer 24

• Inhibiting cell wall synthesis
• Forming pores in the p-membrane leading to lysis
• destroying DNA and RNA (but not destroying our microbiota)
• The trigger to these things is the binding of foreign cells to our own cells
• This innate immune system works with the adaptive immune system.